Please enable JavaScript or talk to your local administrator to get JavaScript enabled.

Project

[Irradiated fibroblast-induced bystander effects on the apoptosis, growth and invasive of urothelial carcinoma under cancer–stromal cell interaction]

Original in Japanese: Irradiated fibroblast-induced bystander effects on the apoptosis, growth and invasive of urothelial carcinoma under cancer–stromal cell interaction

Funder: Japan Society for the Promotion of Science

Funding period
JPY 4.4 M
USD 40 K
Funding amount
Abstract
[With radiation therapy for bladder cancerRadiation-induced bystander Effects of radiation-induced stromal cells on bladder cancer cells are unknown. To elucidate this mechanism, this year we will study the adipose tissue-derived radiation-exposed stromal cells (Adipose tissue stromal cells:以下ATSCs)The intercellular interactions between and non-invasive bladder cancer,collagen gel invasion assay We examined using system. Multiplyki-67, ApoptosisCC3Was evaluated by immunostaining.ATSCsIn the co-culture group with and, the proliferation of non-invasive bladder cancer was suppressed and apoptosis was promoted.ATSCsIn the co-culture group with and, the proliferation of non-invasive bladder cancer was suppressed and apoptosis was promoted. Due to radiation exposurebystander effectによりATSCsが、It was suggested that it could be a growth / invasion suppressor or apoptosis promoting factor for non-invasive cancer cells. Factors involved in the phenomenon of non-invasive bladder cancer in which proliferation is suppressed and apoptosis is promoted,pathwaysBladder cancer-ATSCsProtein extraction and analysis were performed using an interaction analysis model.Phospho-MAPK Proteome Comprehensive analysis with Array,western Expressions were compared by the blots method. Radiation exposureATSCsIn the co-culture group with p- of non-invasive bladder cancerJNKEnhanced expression of,p-p38The suppression of the expression ofJNK, p38などのmoleculesExpression changes ofRadiation-induced bystander It was presumed to be involved in effects. Also, p-AKt, p-mTOR経路のpathwaysExpression was suppressed, and radiation exposureATSCsは、 mTOR It suppressed the expression of the pathway, and this was considered to be one possible mechanism for promoting apoptosis.]
Original in Japanese
膀胱癌に対する放射線療法でRadiation-induced bystander effectsによる放射線被爆間質細胞が膀胱癌細胞に与える影響は不明である。このメカニズム解明のために、今年度は脂肪組織由来放射線被爆間質細胞(Adipose tissue stromal cells:以下ATSCs)と非浸潤性膀胱癌との細胞間相互作用について、collagen gel invasion assay systemを用いて検討を行った。増殖をki-67、アポトーシスをCC3の免疫染色にて評価を行った。ATSCsとの共培養群で、非浸潤性膀胱癌の増殖が抑制され、アポトーシスが促進されたが、放射線被爆ATSCsとの共培養群でより、非浸潤性膀胱癌の増殖が抑制され、アポトーシスが促進された。放射線被曝によるbystander effectによりATSCsが、非浸潤性癌細胞の増殖・浸潤抑制因子、アポトーシス促進因子になることが示唆された。非浸潤性膀胱癌が増殖抑制、アポトーシス促進された現象の関与因子、pathwaysを検討するため、膀胱癌-ATSCs相互作用解析モデルを用い蛋白抽出と解析を行った。Phospho-MAPK Proteome Arrayにて網羅的解析い、western blots法で発現の比較を行った。放射線被爆ATSCsとの共培養群では、非浸潤性膀胱癌のp-JNKの発現亢進、p-p38の発現抑制がそれぞれ促進され、JNK, p38などのmoleculesの発現変化がRadiation-induced bystander effectsに関与することが推測された。また, p-AKt, p-mTOR経路のpathwaysの発現抑制が見られ、放射線被曝ATSCsは、 mTOR 経路の発現を抑制し、これがアポトーシス促進のメカニズムの一つとして可能性が考えられた。
Similar projects All >
Sorted by: Start Date
Project list item
Dissecting myeloid cell-mediated resistance to immune checkpoint blockade in bladder cancer

National Cancer Institute to NINA BHARDWAJ, MATTHEW GALSKY, JUN ZHU

USD 703,400
2020 - 2025
Project list item
Combatting Bladder Cancer by Inducing Epithelial Turnover

National Cancer Institute to SOMAN N ABRAHAM

USD 372,404
2019 - 2021
Project list item
The role of a new molecular driver in bladder cancer

National Cancer Institute to DALEY MORERA

USD 90,032
2018 - 2021
Project list item
Modeling bladder cancer metastasis using human patient-derived tumor organoids

Bladder Cancer Advocacy Network to Michael M Shen

USD 300,000
2018 - 2020
Project list item
Role of B-arrestins in bladder cancer progression and response to chemotherapy

United States Department of Veterans Affairs to BAL L LOKESHWAR

 
2018 - 2022

System

Categories
  • FOR (ANZSRC)

    1112 Oncology and Carcinogenesis

  • RCDC

    Cancer

  • RCDC

    Urologic Diseases

  • HRCS HC

    Cancer

  • HRCS RAC

    2.1 Biological and endogenous factors

  • Health Research Areas

    Biomedical

  • Broad Research Areas

    Basic Science